Explaining rapid reinfections in multiple-wave influenza outbreaks: Tristan da Cunha 1971 epidemic as a case study

Camacho, Anton; Ballesteros, Sébastien; Graham, Andrea L.; Carrat, Fabrice; Ratmann, Oliver; Cazelles, Bernard

A multi-pronged innate [33] and adaptive [34] immune response is optimal for clearing influenza infection. The innate response is the first to be activated and plays a key role through its ability to control early viral replication and to promote and regulate the virus-specific adaptive immune response [33] . Cytokines are among the most important bridges between the innate and adaptive responses to influenza [35] . The adaptive response itself may be broken into two critical sub-components: (i) the cellular immune response by which antigen-specific cytotoxic T lymphocytes (CTLs) eliminate infected cells and thus prevent viral release, and (ii) the humoral immune response by which serum antibodies efficiently neutralize the virus (both of which are promoted by T-cell help [34] ). Antibodies can remain detectable for years after infection and prevent reinfection by the same strain as well as by sufficiently cross-reactive variants [36] . Genetic variation in any of these immune components might determine whether or how rapidly an individual develops protective immunity following primary influenza infection (in keeping with the AoN or Win hypotheses, respectively).